TY - JOUR
T1 - SMN affects membrane remodelling and anchoring of the protein synthesis machinery
AU - Gabanella, Francesca
AU - Pisani, Cinzia
AU - Borreca, Antonella
AU - Farioli-Vecchioli, Stefano
AU - Ciotti, Maria Teresa
AU - Ingegnere, Tiziano
AU - Onori, Annalisa
AU - Ammassari-Teule, Martine
AU - Corbi, Nicoletta
AU - Canu, Nadia
AU - Monaco, Lucia
AU - Passananti, Claudio
AU - Di Certo, Maria Grazia
PY - 2016
Y1 - 2016
N2 - Disconnection between membrane signalling and actin networks can have catastrophic effects depending on cell size and polarity. The survival motor neuron (SMN) protein is ubiquitously involved in assembly of spliceosomal small nuclear ribonucleoprotein particles. Other SMN functions could, however, affect cellular activities driving asymmetrical cell surface expansions. Genes able to mitigate SMN deficiency operate within pathways in which SMN can act, such as mRNA translation, actin network and endocytosis. Here, we found that SMN accumulates at membrane protrusions during the dynamic rearrangement of the actin filaments. In addition to localization data, we show that SMN interacts with caveolin-1, which mediates anchoring of translation machinery components. Importantly, SMN deficiency depletes the plasma membrane of ribosomes, and this correlates with the failure of fibroblasts to extend membrane protrusions. These findings strongly support a relationship between SMN and membrane dynamics. We propose that SMN could assembly translational platforms associated with and governed by the plasma membrane. This activity could be crucial in cells that have an exacerbated interdependence of membrane remodelling and local protein synthesis.
AB - Disconnection between membrane signalling and actin networks can have catastrophic effects depending on cell size and polarity. The survival motor neuron (SMN) protein is ubiquitously involved in assembly of spliceosomal small nuclear ribonucleoprotein particles. Other SMN functions could, however, affect cellular activities driving asymmetrical cell surface expansions. Genes able to mitigate SMN deficiency operate within pathways in which SMN can act, such as mRNA translation, actin network and endocytosis. Here, we found that SMN accumulates at membrane protrusions during the dynamic rearrangement of the actin filaments. In addition to localization data, we show that SMN interacts with caveolin-1, which mediates anchoring of translation machinery components. Importantly, SMN deficiency depletes the plasma membrane of ribosomes, and this correlates with the failure of fibroblasts to extend membrane protrusions. These findings strongly support a relationship between SMN and membrane dynamics. We propose that SMN could assembly translational platforms associated with and governed by the plasma membrane. This activity could be crucial in cells that have an exacerbated interdependence of membrane remodelling and local protein synthesis.
KW - Actin filament
KW - Local translation
KW - Membrane remodelling
KW - SMN
UR - http://www.scopus.com/inward/record.url?scp=84961218545&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84961218545&partnerID=8YFLogxK
U2 - 10.1242/jcs.176750
DO - 10.1242/jcs.176750
M3 - Article
AN - SCOPUS:84961218545
VL - 129
SP - 804
EP - 816
JO - Journal of Cell Science
JF - Journal of Cell Science
SN - 0021-9533
IS - 4
ER -